When functioning properly, the human heart maintains its own intrinsic rhythm, and is capable of pumping adequate blood throughout the body's circulatory system. However, some people have irregular cardiac rhythms, referred to as cardiac arrhythmias. Such arrhythmias result in diminished blood circulation. One manner of treating cardiac arrhythmias includes the use of a cardiac rhythm management system. Such systems can be implanted in a patient to deliver electrical pulses to the heart.
Cardiac rhythm management systems include, for example, pacemakers (also referred to as “pacers”), defibrillators (also referred to as “cardioverters”) and cardiac resynchronization therapy (“CRT”) devices. These systems use conductive leads having one or more electrodes to deliver pulsing energy to the heart, and can be delivered to an endocardial, epicardial and myocardial position within the heart.
Unfortunately, interactions between the electrode and the adjacent tissue in the heart may vary the stimulation thresholds of the tissue over time. This variation can be caused by the formation of fibrotic scar tissue during the recovery and healing process as the body reacts to the presence of the electrode. The formation of fibrotic tissue may result in chronic stimulation energy thresholds that exceed the acute energy thresholds obtained immediately after implant. As a result, higher stimulation energies are required, thereby shortening the usable life of the battery-powered implantable cardiac rhythm management device.
To inhibit the growth of scar tissue, leads have been configured to release active agents such as steroids in the vicinity of the electrode. For example, drug eluting collars have been placed adjacent to electrodes to inhibit the growth of scar tissue. One challenge with drug eluting collars and other drug release structures is that it is difficult to control both the amount of drug being released and the amount of drug that ultimately reaches the affected tissue site.